Gene Rv3133c (dosR)
in Mycobacterium tuberculosis H37Rv
General annotation
Type | CDS |
Function | Regulator part of the two component regulatory system DEVR/DEVS/dost. Controls HSPX|Rv2031|ACR expression. |
Product | Two component transcriptional regulatory protein DevR (probably LuxR/UhpA-family) |
Comments | Rv3133c, (MTCY03A2.25), len: 217 aa. DevR (alternate gene name: dosR), two component transcriptional regulator (see Dasgupta et al., 2000; dev for Differentially Expressed in Virulent strain), highly similar to several e.g. O85372|CPRR two component regulator from Rhodococcus sp. (212 aa), FASTA scores: opt: 868, E(): 6.2e-46, (65.05% identity in 206 aa overlap); Q9RI42|SCJ12.16c putative LuxR family two-component response regulator from Streptomyces coelicolor (233 aa), FASTA scores: opt: 849, E(): 9.7e-45, (60.55% identity in 218 aa overlap); Q9XA59|SCGD3.19 putative two-component system response transcriptional regulator from Streptomyces coelicolor (218 aa), FASTA scores: opt: 835, E(): 6.5e-44, (61.55% identity in 208 aa overlap); and similar to others. Contains bacterial regulatory proteins, LuxR family signature (PS00622) near C-terminus as seen in bvgA, comA, dctR, degU, evgA, fimZ, fixJ, gacA, glpR, narL, narP, nodW, rcsB and uhpA. Helix-turn-helix motif at 166-187 (+3.15 SD). Belongs to the LuxR/UhpA family of transcriptional regulators. The N-terminal region is similar to that of other regulatory components of sensory transduction systems. |
Functional category | Regulatory proteins |
Proteomics | The product of this CDS corresponds to spot 3_305 identified in culture supernatant by proteomics at the Max Planck Institute for Infection Biology, Berlin, Germany, and also at the Statens Serum Institute (Denmark) (see proteomics citations). Identified in the membrane fraction of M. tuberculosis H37Rv using 1D-SDS-PAGE and uLC-MS/MS (See Gu et al., 2003). Identified in the culture supernatant of M. tuberculosis H37Rv using mass spectrometry (See Mattow et al., 2003). Identified in the cytosol and cell membrane fraction of M. tuberculosis H37Rv using 2DLC/MS (See Mawuenyega et al., 2005). Identified in the membrane fraction of M. tuberculosis H37Rv using nanoLC-MS/MS (See Xiong et al., 2005). Identified by mass spectrometry in Triton X-114 extracts of M. tuberculosis H37Rv (See Malen et al., 2010). Identified by mass spectrometry in the membrane protein fraction and whole cell lysates of M. tuberculosis H37Rv but not the culture filtrate (See de Souza et al., 2011). |
Transcriptomics | mRNA identified by DNA microarray analysis: gene induced by hypoxia (see Sherman et al., 2001), under microaerobic and anaerobic conditions (see Mayuri et al., 2002), and down-regulated after 4h of starvation (see Betts et al., 2002). |
Mutant | Non-essential gene for in vitro growth of H37Rv in a MtbYM rich medium, by Himar1 transposon mutagenesis (see Minato et al. 2019). Non-essential gene for in vitro growth of H37Rv, by analysis of saturated Himar1 transposon libraries (see DeJesus et al. 2017). Non essential gene by Himar1 transposon mutagenesis in H37Rv strain (see Sassetti et al., 2003). Non-essential gene for in vitro growth of H37Rv, by Himar1 transposon mutagenesis (See Griffin et al., 2011). M. tuberculosis H37Rv mutant is attenuated in guinea pigs (See Malhotra et al., 2004). M. tuberculosis H37Rv mutant shows increased virulence in SCID mice; mutant grows more quickly in DBA mice and in IFN-gamma activated macrophages (See Parish et al., 2004). Check for mutants available at TARGET website |
Coordinates
Type | Start | End | Orientation |
---|---|---|---|
CDS | 3499262 | 3499915 | - |
Genomic sequence
Feature type
Upstream flanking region (bp)
Downstream flanking region (bp)
Update
Protein sequence
>Mycobacterium tuberculosis H37Rv|Rv3133c|devR VVKVFLVDDHEVVRRGLVDLLGADPELDVVGEAGSVAEAMARVPAARPDVAVLDVRLPDGNGIELCRDLLSRMPDLRCLILTSYTSDEAMLDAILAGASGYVVKDIKGMELARAVKDVGAGRSLLDNRAAAALMAKLRGAAEKQDPLSGLTDQERTLLGLLSEGLTNKQIADRMFLAEKTVKNYVSRLLAKLGMERRTQAAVFATELKRSRPPGDGP
Bibliography
- Jungblut PR, Schaible UE, Mollenkopf HJ, Zimny-Arndt U, Raupach B, Mattow J, Halada P, Lamer S, Hagens K and Kaufmann SH [1999]. Comparative proteome analysis of Mycobacterium tuberculosis and Mycobacterium bovis BCG strains: towards functional genomics of microbial pathogens. Proteomics
- Mollenkopf HJ et al. [1999]. A dynamic two-dimensional polyacrylamide gel electrophoresis database: the mycobacterial proteome via Internet. Proteomics
- Dasgupta N et al. [2000]. Characterization of a two-component system, devR-devS, of Mycobacterium tuberculosis. Biochemistry Regulation
- Sherman DR, Voskuil M, Schnappinger D, Liao R, Harrell MI and Schoolnik GK [2001]. Regulation of the Mycobacterium tuberculosis hypoxic response gene encoding alpha -crystallin. Transcriptome
- Betts JC et al. [2002]. Evaluation of a nutrient starvation model of Mycobacterium tuberculosis persistence by gene and protein expression profiling. Transcriptome
- Mayuri et al. [2002]. Molecular analysis of the dormancy response in Mycobacterium smegmatis: expression analysis of genes encoding the DevR-DevS two-component system, Rv3134c and chaperone alpha-crystallin homologues. Product Transcriptome
- Park HD et al. [2003]. Rv3133c/dosR is a transcription factor that mediates the hypoxic response of Mycobacterium tuberculosis. Mutant Function Transcriptome
- Voskuil MI, Schnappinger D, Visconti KC, Harrell MI, Dolganov GM, Sherman DR and Schoolnik GK [2003]. Inhibition of respiration by nitric oxide induces a Mycobacterium tuberculosis dormancy program. Regulon
- Sassetti CM et al. [2003]. Genes required for mycobacterial growth defined by high density mutagenesis. Mutant
- Florczyk MA et al. [2003]. A family of acr-coregulated Mycobacterium tuberculosis genes shares a common DNA motif and requires Rv3133c (dosR or devR) for expression. Regulation Secondary
- Parish T et al. [2003]. Deletion of two-component regulatory systems increases the virulence of Mycobacterium tuberculosis. Mutant Secondary Function
- Gu S et al. [2003]. Comprehensive proteomic profiling of the membrane constituents of a Mycobacterium tuberculosis strain. Proteomics
- Mattow J, Schaible UE, Schmidt F, Hagens K, Siejak F, Brestrich G, Haeselbarth G, Muller EC, Jungblut PR and Kaufmann SH [2003]. Comparative proteome analysis of culture supernatant proteins from virulent Mycobacterium tuberculosis H37Rv and attenuated M. bovis BCG Copenhagen. Proteomics
- Roberts DM et al. [2004]. Two sensor kinases contribute to the hypoxic response of Mycobacterium tuberculosis. Function
- Malhotra V et al. [2004]. Disruption of response regulator gene, devR, leads to attenuation in virulence of Mycobacterium tuberculosis. Mutant
- Saini DK et al. [2004]. DevR-DevS is a bona fide two-component system of Mycobacterium tuberculosis that is hypoxia-responsive in the absence of the DNA-binding domain of DevR. Function
- Xiong Y, Chalmers MJ, Gao FP, Cross TA and Marshall AG [2005]. Identification of Mycobacterium tuberculosis H37Rv integral membrane proteins by one-dimensional gel electrophoresis and liquid chromatography electrospray ionization tandem mass spectrometry. Proteomics
- Mawuenyega KG et al. [2005]. Mycobacterium tuberculosis functional network analysis by global subcellular protein profiling. Proteomics
- Wisedchaisri G et al. [2005]. Structures of Mycobacterium tuberculosis DosR and DosR-DNA complex involved in gene activation during adaptation to hypoxic latency. Structure
- MÃ¥len H et al. [2010]. Definition of novel cell envelope associated proteins in Triton X-114 extracts of Mycobacterium tuberculosis H37Rv. Proteomics
- Griffin JE et al. [2011]. High-resolution phenotypic profiling defines genes essential for mycobacterial growth and cholesterol catabolism. Mutant
- de Souza GA et al. [2011]. Bacterial proteins with cleaved or uncleaved signal peptides of the general secretory pathway. Proteomics
- DeJesus MA et al. [2017]. Comprehensive Essentiality Analysis of the Mycobacterium tuberculosis Genome via Saturating Transposon Mutagenesis. Mutant
- Minato Y et al. [2019]. Genomewide Assessment of Mycobacterium tuberculosis Conditionally Essential Metabolic Pathways. Mutant